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photo of Irving coy Allen

Assistant Professor, Department of Biomedical Science

Program Focus

What are the critical factors associated with the initiation and resolution of inflammation? Likewise, dysregulated inflammation is directly associated with a myriad of human and veterinary diseases, including cancer. Indeed dysregulation of inflammation is a hallmark feature of cancer and is a critical element associated with the tumor microenvironment. How can we control or modulate the immune system during tumorigenesis and maintain immune system homeostasis to improve patient outcomes? These are the questions that my laboratory is attempting to address. As an immunologist, my research program is focused on exploring the intersection between the immune system and cancer. Specifically, we are interested in understanding the contribution of unique families of pattern recognition receptors (PRRs) in modulating disease pathogenesis and inflammatory microenvironments. PRRs are proteins that recognize pathogen-associated molecular patterns (PAMPs), which are present within viruses, bacteria, and other microbial species. PRRs are also responsible for sensing damage-associated molecular patterns (DAMPs), which are produced by host cells under a variety of pathologic conditions to coordinate the immune response to cellular damage and/or stress. PAMPs and DAMPs are recognized by three major classes of PRRs studied in my laboratory: the Toll-like receptors (TLRs); retinoic acid inducible gene-I (RIG-I)-like receptors (RLRs); and the nucleotide-binding domain-leucine-rich repeat-containing molecules (“NOD-like” receptors; NLRs). These three protein families and their respective signaling cascades form the foundation of the innate immune system and play critical roles in protecting the host.

Allen Lab Website

Selected Publications

1.     Allen,I.C., Wilson,J.E., Schneider, M., Lich,J.D., Authur,J.C., Woodford,R.M., Uronis,J.M.,           Davis,B.K., Roberts,R.A., Rogers,A.B., Herfarth,H.H., Jobin,C.,    and Ting, J.P.Y.          (2012). NLRP12 Functions as a Negative Regulator of          Noncanonical NF-κB   Signaling and Tumorigenesis during Colitis Associated Cancer. Immunity. May          25;36(5):742-54. PubMed PMID: 22503542

2.     Williams, T.M. Leeth R.A., Rothschild D.E., Coutermarsh-Ott, S.L., McDaniel      D.K.,    Simmons A.E., Heid B., Cecere T.E., Allen,I.C. (2015). The NLRP1      Inflammasome Attenuates Colitis and Colitis-Associated Tumorigenesis. The      Journal of Immunology. Apr 1;194(7):3369-80. PMID: 25725098.

3.     Coutermarsh-Ott, S.L., Simmons, A., Capria, V., LeRoith, T., Wilson, J.E.,      Heid,    B.,        Washington, C., Qin, Q., Ting, J., Hontecillas-Magarzo, R.,      Bassaganya-Riera, J.,            Dervisis, N., Allen, I.C. (2016). NLRX1 Suppresses           Tumorigenesis and     Attenuates       Histiocytic Sarcoma through the Negative        Regulation of NF-κB   Signaling.        Oncotarget. May 31;7(22):33096-110. PMID:          27105514.

4.     Rothschild, D.E., Zhang, Y., Diao, N., Lee, C., Chen, K., Caswell, C.C., Slade,      D.J., Helm, R.F., LeRoith,       T., Li, L., Allen, I.C. (2016). Enhanced mucosal      defense and reduced tumor burden in mice with the compromised negative      regulator IRAK-M. EBioMedicine. Feb;15:36-47.